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At least 217 records · Page 12Linked to original sources

[Ergotamine poisoning. Two cases of peripheral ischemia].

Ergotism is a rare disorder, generally caused by iatrogenia after the administration of drugs containing ergotamine derivates. Two cases of ischemic incidents at the extremities caused by a chronic intoxication with ergotamine tartrate, after its prolonged administration in therapeutical doses as a treatment for hemicrany, are reported. A short bibliographic review about semiology and therapeutic possibilities of such toxic pathology has been made.

Adult↗

Severe vascular spasm due to erythromycin-ergotamine interaction.

We report a case of ergotism due to the interaction of erythromycin with a small dose of ergotamine tartrate (2 mg). Besides severe peripheral vasospasm with dysaesthesiae there was transient renal ischaemia. Recovery occurred after several weeks without sodium nitroprusside therapy. Cases previously reported in the literature are reviewed.

Acne Vulgaris↗

Bilateral focal cortical atrophy and chronic ergotamine abuse.

A 67-year-old patient took 5 mg of ergotamine daily for 18 months. His headaches and dysphoria were greatly improved by stopping this drug. Brain imaging by CT and magnetic resonance techniques showed numerous atrophic lesions that may represent infarcts due to occlusion of superficial cortical vessels.

Aged↗

[Non-tropical sprue and chronic inflammatory rectal stenosis in a patient with abuse of ergotamine-containing suppositories].

A 51 year old Yugoslavian patient was admitted to our hospital in reduced general condition with distinct hypocalcemia, osteomalacia, and with rectum stenosis. Our investigations led to the diagnosis of a malabsorption syndrome due to non-tropical sprue. The most likely cause of the rectum stenosis is an abuse of ergotamine-containing suppositories for several years. A gluten-free diet and the interruption of the use of the suppositories improved her general condition remarkably.

Bone Density↗

[Ergotamine induced ischemia].

Drugs containing ergotamine are commonly used in the treatment of migraine. Hypersensitivity to these drugs may be triggered off even with intake of recommended doses, inducing peripheral ischemia. Contributing factors to ergotism are concurrent fever, liver disease and drugs such as erythromycin or propranolol. We present a case history and different methods of treatment.

Ergotamine↗

Evaluation of physiologic indices in mice vaccinated with protein-ergotamine conjugates and fed an endophyte-infected fescue diet.

OBJECTIVES: To assess effects of vaccination against fescue toxicosis on weight gain, serum prolactin and cholesterol concentrations, and alkaline phosphatase (ALP) activity in mice fed an endophyte-infected (EI) or endophyte-free (EF) fescue diet. ANIMALS: 50 six-week-old male BALB/c mice. PROCEDURE: Mice were randomly allocated to the following 5 groups: 1, vaccinated intraperitoneally with a bovine serum albumin-ergotamine (EG) conjugate and fed an EI fescue diet; 2, orally vaccinated with cholera toxin (CT) subunit B-EG conjugate mixed with free CT and fed an EI fescue diet; 3, not vaccinated and fed an EI fescue diet; 4, passively vaccinated with monoclonal antibodies specific for ergovaline (EV) and fed an EI fescue diet; and 5, not vaccinated and fed an EF fescue diet. RESULTS: Antibodies against EG and EV were in serum of mice of groups 1 and 4, respectively. Secretory IgA and IgG coproantibodies against EG were induced in mice of group 2. Weight increased in groups 1 and 2 and tended to be increased in group 4 versus group 3. Prolactin concentration was similar in all groups; cholesterol concentration was decreased in groups 1, 3, and 4, compared with group 5. Compared with that in group 5, serum ALP activity decreased in groups 1 and 4 and was further decreased in group 1, compared with that in groups 2 and 3; it was negatively correlated with anti-EG titer. CONCLUSIONS AND CLINICAL RELEVANCE: Induction of anti-EG antibodies and administration of EV monoclonal antibodies tended to increase short-term weight gain in this murine model of fescue toxicosis. However, systemic IgG antibodies against EG or EV antibodies were not protective against decreases in serum ALP activity and cholesterol concentrations. Clinical significance of decreased ALP activity associated with vaccination is unknown, but represents a worsening of a response often associated with fescue toxicosis in cattle.

Acremonium↗

Responsiveness of isolated canine cerebral and peripheral arteries to ergotamine.

Changes in tension of spiral strips from dog saphenous, external carotid and basilar arteries were monitored isometrically. Serotonin (5-HT) contracted the 3 arterial preparations in about the same concentration range. Compared with noradrenaline (NA) (100%) the efficacy of 5-HT was about 60% on saphenous, 150% on external carotid and about 500% on basilar arteries. Ergotamine (E) stimulated the 3 vascular preparations in concentrations about 100 times lower than 5-HT. Compared with NA the efficacy of E was about 20% on saphenous, 50% on external carotid and 200% on basilar arteries. Compared with 5-HT (100%) however, E had similar constrictor activities in the 3 arteries. It seemed likely therefore that 5-HT receptors are involved in the vasoconstrictor activity of E. Evidence for this was obtained in experiments in which cyproheptadine (Cy), a 5-HT antagonist, was used. For antagonism of E concentrations of Cy about 6 times higher than those required to inhibit 5-HT were necessary, whereas for antagonism of NA about 500 times higher Cy concentrations were necessary. The results suggest that on canine arterial vascular smooth muscle the constrictor activity of E is mediated mainly through serotoninergic receptor sites.

Animals↗

Failure of ergotamine to act as an amplifier of sulfonylurea-stimulated insulin secretion.

Normal dogs were injected i.v. with 0.25 mg/kg sodium salt of HB 419 (glibenclamide) and plasma insulin concentrations were measured over a period of 2 hrs. When the animals were given a single i.v. injection of 0.2 mg/kg dihydroergotamine tartrate (DHE) 30 min prior to the administration of HB 419, the insulinogenic effect of the sulfonylurea was considerably amplified (192 muU/ml vs 34 muU/ml at 45 min). No augmentation of the insulinogenic effect of HB 419 was observed when the same experiments were conducted with 0.05, 0.025 or 0.01 mg/kg ergotamine tartrate. At the dose level of 0.1 mg/kg the insulinogenic effect of HB 419 was suppressed. Since the structural difference between these two ergot alkaloids consists of the presence or absence of the double bond at C9 and C10 of the lysergic acid moiety, it appears that saturation of this double bond is an essential structural requirement for DHE to function as an amplifier of sulfonylurea-stimulated insulin release.

Animals↗

Acute coronary syndrome associated with myocardial bridging due to ergotamine treatment for migraine.

A 48-year-old woman presented with acute coronary syndrome and underwent coronary angiography which revealed myocardial bridging at the distal end of the left anterior descending artery with otherwise normal coronary arteries. The patient used to take ergotamine for her chronic migraine. Possible association with myocardial bridging which was found in this patient is discussed.

Acute Disease↗

Buccal absorption of ergotamine tartrate using the bioadhesive tablet system in guinea-pigs.

The buccal administration of ergotamine tartrate (ET) combined with polyvinyl alcohol (PVA) gel brought about higher plasma concentration of ET compared with that of oral administration of capsules in guinea-pigs. T(max) of ET in plasma of buccal administration was significantly smaller than that of oral administration. For the buccal dosage form of ET, the bioadhesive tablet system (BTS) was newly developed. It consisted of a reservoir of drug and an adhesive region. BTS showed better absorption of ET compared with PVA gel in guinea pigs. Among several pharmaceutical bases in the reservoir of BTS, Witepsol W-35 was most effective. It is likely that the high lipophilic property of Witepsol W-35 in which ET was dissolved facilitated the drug release by its relatively low melting point (around 35 degrees C), consequently a rapid absorption. In addition, the enhancing activity of the cod-liver oil extract (CLOE) in hydrophilic ointment on the in vivo buccal ET absorption was clarified to be comparable to that in the in vitro study utilizing the keratinized epithelial-free membrane (KEF-membrane) of the hamster cheek pouch.

Absorption↗

Rapid reversal of ergotamine-induced vasospasm.

Peripheral ischemia, secondary to ergotamine tartrate and caffeine suppositories is reported in a 48-year-old female. Lower extremity pre-gangrenous changes were unresponsive to surgical sympathectomy, calcium channel blockade, intra-arterial vasodilators and systemic anticoagulation. A dramatic clinical and radiological reversal of the vasospasm was obtained with intravenous sodium nitroprusside when surgical amputation appeared inevitable.

Angiography↗

The early use of ergotamine in migraine. Edward Woakes' report of 1868, its theoretical and practical background and its international reception.

Although ergot had been used in obstetrics for several centuries, it was proposed for the treatment of migraine only in the 19th century. The British ENT-surgeon Edward Woakes (1837-1912) recommended ergot as a vasoconstricting agent for migraine and other neurogenic conditions associated with vasodilatation in 1868. He subscribed to the theory of vasodilatation by sympathetic deficit, presented in the early 1850s by Brown-Séquard and Claude Bernard. Du Bois-Reymond proposed vasoconstriction by sympathetic overactivity as the cause of migraine in 1860; Brown-Séquard opposed this in favour of vasodilatation. Vasodilatation due to sympathetic deficit in migraine was again supported by Möllendorf, with clinical evidence, in 1867. Woakes' paper of 1868 introduced ergot as a vasoconstrictor for the same condition. Reception abroad was prompt. A German version appeared in 1869, and Eulenburg cited Woakes in his textbook of 1871. Eulenburg presented the use of ergot for migraine as a routine measure in the second edition of his textbook in 1878, and in a paper published in 1883. The method was internationally accepted, but it became really popular only after the isolation of pure ergotamine in 1918, resulting in the first reliable compounds with stable properties and predictable effects. Contrary to Woakes' theory, in the early 20th century ergot was used for migraine because of its well-documented adrenolytic properties, as migraine was by then again believed to be a sympathotonic and vasospastic condition.

England↗

[Myocardial infarct during ergotamine medication in a young man with normal coronary arteries].

Normal coronary vessels and an akinetic anterolateral wall segment were found in a 24-year-old patient on angiography 10 months after a clinically established myocardial infarction. As the patient had been on a high-dosage medication with ergotamine for two years and as all risk factors for coronary sclerosis as well as evidence of other cardiac diseases were lacking, it seems appropriate to assume that myocardial ischaemia had been caused by coronary spasms.

Adult↗

Irreversible coma, ergotamine, and ritonavir.

We report the first case in the medical literature (to our knowledge) of a patient with human immunodeficiency virus infection who was being treated with ritonavir and developed signs of severe vascular involvement and irreversible coma after the administration of 3 mg of ergotamine tartrate.

Adult↗